Rapid enlargement of subdural haematoma.
RD Bhavani, TD Nadkarni, AP Karapurkar
Dept of Neurosurgery, Seth GS Medical College, Parel, Bombay, Maharashtra.
R D Bhavani
Dept of Neurosurgery, Seth GS Medical College, Parel, Bombay, Maharashtra.
A case of subdural haematoma (SDH) having atypical features (headache, vomiting, drowsiness but normal haematological and metabolic parameters and no localising neurological signs) is reported. The SDH rapidly enlarged and liquefied in five days as evident on computerised tomographic (CT) scan and operative findings. Rapid improvement was observed following this. Abnormally excessive fibrinolytic activity in the SDH is a possible cause.
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Bhavani R D, Nadkarni T D, Karapurkar A P. Rapid enlargement of subdural haematoma. J Postgrad Med 1994;40:35-7
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Bhavani R D, Nadkarni T D, Karapurkar A P. Rapid enlargement of subdural haematoma. J Postgrad Med [serial online] 1994 [cited 2020 Feb 19 ];40:35-7
Available from: http://www.jpgmonline.com/text.asp?1994/40/1/35/573
Subdural haematomas (SDH) occur due to haemorrhage into the dura-arachnoid interface. Small, acute SDH resolve spontaneously or progress to chronic SDH over a period of three weeks. The progression of acute SDH to chronic SDH within days is rare. We are presenting one such case.
A 62-year-old male was admitted with severe right frontal throbbing headaches. He vomited and became unconscious. There was no history of trauma or any other major illness. On examination, only the felt plantar was equivocal. The haematological profile was normal. All other metabolic parameters were within normal limits. The CT Scan [Figure:1] showed small, crescentic, hyperdense, right-sided acute SDH with minimal midline shift.
The patient was kept under close clinical observation. After four days he became extremely drowsy and arousable only after coaxing. He had no localising neurological signs. A repeat CT Scan [Figure:2] showed the reduced hyperdense acute SDH clot and in addition a large, hypodense, right, chronic SDH with significant midline shift to the left and compression of ipsilateral ventricle.
A right parietal burr hole yielded approximately 100 ml liquid haematoma. The patient remained drowsy for a day and then showed rapid improvement.
Subdural haematomas are divided into three types depending on the presentation and chronological age. 1. Acute SDH presentation with 72 hours. 2. Subacute SDH presentation with 3 days to 3 weeks and 3. Chronic SDH presentation with 3 weeks to months.
The aetiological factor for the origin and development of chronic SDH has been debated since Virchow reported “pachymeningitis haemorrhagica interna” in 1857. In order to explain the mechanism the osmotic gradient theory was proposed by Gardner. However, Weir, proved that there is no significant difference in osmotic pressure between haematoma fluid, venous blood and cerebrospinal fluid and in the oncotic pressure between haematoma fluid and venous blood.
Recurrent haemorrhage from haematoma capsule was proposed. The vessels of haematoma capsule were reported to have marked proliferative potential and are fragile,,. However, recurrent haemorrhage from haematoma capsule theory does not explain how haematoma fluid accumulates during the early stage before the formation of vascular outer membrane. In addition simple drainage of haematoma leaving the entire outer membrane in situ is curative in most cases.
A recent study of the coagulation and fibrinolytic profile of evacuated clot has indicated that there is excessive activation of clotting system, thrombin generation and increased fibrinolytic activity occurring in the haematoma fluid as compared to intravascular blood. However, the exact reason of this localised manifestation of altered clotting fibrinolytic system within the subdural space in the absence of generalised manifestations remains an enigmag. This could be a possible aetiological factor for origin and development of chronic SDH as follows. Damage to cerebral endothelia, blood cells and brain tissue releases abundant tissue thromboplastin in subdural space. The clotting systems are excessively activated resulting in marked consumption of clotting proteins. An excessive activation of the intrinsic clotting system leads to excessive activation of intrinsic fibrinolytic systems. The cross-linked fibrin polymer is degraded to form fibrinogen degradation products (FDP) and defective clot formation causes recurrent -haemorrhage in the damaged area. As the process is repeated the dura reacts non-specifically to form the vascularised outer membrane gradually. As the outer membrane proliferates, the extrinsic fibrinolytic system is activated and a self-perpetuating vicious cycle is accelerated. The burr hole drainage removes these self-perpetuating factors and restores normal haemostatic mechanism in the subdural space, leading to a cure.
The chronological evaluation of pathological events correlated with CT scan is well-documented [Table:1] ,,
The density of subdural haematoma decreases with increasing age of haematoma. As the process of lysis of red blood cells (RBC) and liquefaction of clot progresses over weeks the CT appearance changes through hyperdense (acute), isodense (subacute) and hypodense (chronic) extra cerebral collection.
Our patient had many atypical features when compared to normal events as given in [Table:1]. The patient deteriorated in lour days due to an abnormally rapid increase in the size of the clot. The CT scan appearance changed from hyperdense to predominantly hypodense in five days. The earliest change in appearance from hyper to isodense documented in literature is two weeks. The patient had no coagulopathy. This rapid increase was not due to haemorrhage in the clot, as a fresh haemorrhage would have been hyperdense. The patient was not anaemic (haemoglobin: 14 gm%) to render the clot hyperdense due to reduced haemoglobin content. Thus it appears that in our patient the fibrinolytic activity has acted abnormally fast to liquefy the clot that which would have occurred in three weeks has occurred in five days. The burr hole drainage of liquid ‘crank case oil’ appearance haematoma verified the fact. Furthermore the haematoma did not have the typical peripheral membrane encountered in chronic SDH.
This case emphasises the need for reinvestigating a patient who harbours a subdural haematoma and has neurological deterioration under observation.
Ramamurthi B. Acute subdural haematoma. In: Vinken PJ, Bruyn GW, editors. Handbook of Clinical Neurology 1976; 24:275-296.|
|2||Virchow R. Das hematoma der dura mater. Verh Phys-Med Ges Wurzburg 1957; 7:134-142.|
|3||Gardner M. Traumatic subdural haematoma with particular reference to the latent interval. Arch Neurol Psychiatr 1932; 27:847-858.|
|4||Weir B. Oncotic pressure of subdural fluids. J Neurosurg 1980; 53:512-515.|
|5||Weir B. The osmolality of subdural haematoma fluid. J Neurosurg 1971; 34:528-533.|
|6||Sato S, Suzuki J. Ultrastructure observations of the capsule of chronic subdural haematoma in various clinical stages. J Neurosurg 1975; 43:569-578.|
|7||Yamashima T, Kubota T, Yamamoto S. Eosinophil degranulation in the capsule of chronic subdural haematomas. J Neurosurg 1985; 62:257-260.|
|8||Yamashima T, Yamamoto S. How do vessels proliferate in the capsule of a chronic subdural haematoma ? Neurosurgery 1984; 15:672-678.|
|9||Kawakami T, Chikama M, Tamiya T, Shimamura Y. Coagulation and fibrinolysis in chronic subdural haematoma. Neurosurgery 1989; 25:25-29.|
|10||Hardman M. The pathology of traumatic brain injuries. Adv Neurol 1979: 22:15-50.|
|11||Kaufman HH, Singer GM, Sadhu VK. Isodense acute subdural hematoma. J Comput Assist Tomogr 1979; 45:217-224.|
|12||Messina AV, Chernick NL. Computed tomography: the “resolving” intracerebral haemorrhage. Radiology 1976; 118:609-613.|